Noda Y, Kimura H, McGeer P L
Brain Res. 1981 Jun 15;214(2):451-4. doi: 10.1016/0006-8993(81)91211-7.
In in vitro incubations, kainic acid-lesioned neostriatal slices from rat brain showed decreases in oxygen consumption (50%) and in the conversion of both [1-14C]glucose (43%) and [6-14C]glucose (69%) to 14CO2 as compared to controls. The elevation in the C1/C6 14CO2 ratio suggested the pentose phosphate pathway was less affected than the Embden-Meyerhof path in kainic acid-injected gliotic tissue. Increasing the potassium concentration from 6 to 50 mM caused increases in oxygen consumption and glucose utilization in both control and kainic acid-lesioned neostriatal slices; this is consistent with, but not conclusive of, a potassium-stimulating effect on glial as well as neuronal metabolism.
在体外培养中,与对照组相比,来自大鼠脑的红藻氨酸损伤的新纹状体切片显示出氧气消耗减少(50%),以及[1-14C]葡萄糖(43%)和[6-14C]葡萄糖(69%)向14CO2的转化减少。C1/C6 14CO2比率的升高表明,在注射红藻氨酸的胶质化组织中,磷酸戊糖途径受影响程度小于糖酵解途径。将钾浓度从6 mM增加到50 mM会导致对照组和红藻氨酸损伤的新纹状体切片中的氧气消耗和葡萄糖利用增加;这与钾对神经胶质细胞以及神经元代谢的刺激作用一致,但并非结论性证据。